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Yr3 Medicine- Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

State the tachyarrhythmias you need to know

A

Supraventricular tachycardias

  • Sinus node
    • Sinus tachycardia
  • Atria
    • Atrial fibrillation
    • Atrial flutter
    • Atrial tachycardia
  • AV node
    • AV nodal re-entrant tachycardia
    • Atrio-ventricular re-entrant tachycardia

Ventricular Tachycardias

  • Ventricular tachycardia (monomorphic)
  • Torades de pointes (polymorphic VT)
  • Ventricular fibrillation
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2
Q

What is the commonest cardiac arrhythmia encountered in clinical practise?

A

Atrial fibrillation

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3
Q

Does prevalence of AF increase with age?

A

Prevelance of AF increases with ageadn the incidence of AF is suspected to increase steadily

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4
Q

AF can be described as paroxysmal, persistent or permanent- describe each

A
  • Paroxysmal: intermittent episodes which self-terminate in 7 days (typically self terminate in <24hrs)
  • Persistent: prolonged episodes that can be terminated by electrical or cardioversion (last >7 days)
  • Permanent: cannot be cardioverted or if attempts to do so are deemed inappropriate
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5
Q

Describe the pathophysiology of AF

A
  • Complex arrhythmia characterised by both abnormal automatic firing and presence of multiple interacting re-entry circuits around atria
  • The disorganised electrical activity overrides normal organised activity from SA node
  • This is leads to uncoordinated, rapid and irregular contraction of atria
  • The AV node responds/conducts impulses intermittently leading to irregular contraction of ventricles
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6
Q

State some risk factors/causes of AF

*HINT: the atrial fibs

A
  • Thyrotoxicosis
  • Hypothermia, hypertension, heart failure
  • Embolism (PE)
  • Alcohol
  • Trauma (cardiac)
  • Recent surgery (cardiac)
  • Ischaemia or infarct
  • Atrial enlargement
  • Lone or idiopathic
  • Fever, anaemia, high output
  • Infection (e.g. sepsis)
  • Bad valves (e.g. mitral stenosis)
  • Stimulants (e.g. cocaine, amphetamine, caffeine)
  • ****NOTE: there are lots of causes for AF. Can use mneumonic but also useful to structure via systems as in the image below.*
  • ***Can also use Mrs SMITH from ZtoF: sepsis, mitral valve pathology, ischaemic heart disease, thyrotoxicosis, hypertension*
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7
Q

Describe the typical presentation of AF

A

Pts often asymptomatic and AF picked up incidentally; however, pts may experience:

  • Palpitations
  • Dyspnoea
  • Syncope (dizziness or fainting)
  • Chest pain
  • Symptoms of associated conditions (e.g. sepsis, stroke, heart failure, thyrotoxicosis etc..)
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8
Q

What might you find on clinical examination of someone with AF?

A
  • Irregularly irregular pulse
  • Tachycardic
  • 1st heart sound of variable intensity
  • Signs of underlying cause (e.g. heart failure, thyrotoxicosis, PE, mitral valve disease)
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9
Q

What other arrhythmia could an irregularly irregular pulse be (aside from AF)?

A

Ventricular ectopic beats

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10
Q

What investigations would you do for suspected AF, include:

  • Bedside
  • Bloods
  • Imaging

*Justify each where appropriate

A

Bedside

  • ECG: show AF

Bloods

  • FBC: raised WCC in infection
  • U&Es: assess electrolytes & can be helpful for choosing anti-arrhythmic
  • TFTs: thyrotoxicosis may present as AF
  • Cardiac enzymes: myocardial ischaemia may be caue of AF
  • NT-pro BNP: suspect heart failure as cause

Imaging

  • CXR: may show precipitating factor such as pneumonia, heart failure
  • ECHO: help identify cause e.g. mitral valve pathology, heart failure
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11
Q

Describe what you would see on the ECG of AF

A
  • Rate: tachycardia
  • Rhythm: irregularly irregular
  • P waves: absent
  • QRS: <120ms
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12
Q

If paroxysmal AF is considered, what further investigations would you want?

A
  • Short term cardiac monitoring with 24hr cardiac monitor (symptoms would have to be very freuqent for you to catch the arrhythmia)
  • AliveCor app/cardiac monitor (often used in primary care)
  • Prolonged cardiac monitoring such as Holter monitor or implantable loop recoder
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13
Q

State the two main principles in the treatment of AF

A
  • Rate or rhythm control
    • Rhythm control means putting back in sinus rhythm. This could be through a single cardioversion event (which can be electrical or pharmacological) or long term medical rhythm control using medications
  • Anticoagulation to prevent stroke
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14
Q

Explain why we want to control the rate in AF

A
  • In AF, atria ‘quiver’ this means ventricles don’t fill with blood as efficiently
  • Furthermore, since heart rate is higher in AF ventricles have less time to fill- further decreasing the effectiveness of ventricular filling in AF
  • Since ventricular filling isn’t as efficient, pre-load decreases resulting in decreased SV and cardiac output
  • Decreased CO can lead to myocardial ischaemia and potentially infarct
  • Aim of rate control is to get HR <100bpm to increase time for ventricular filling
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15
Q

What are the two main options for rhythm control in AF?

A
  • Cardioversion (electrical or pharmacological)
  • Long term medical rhythm control
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16
Q

NICE (2014 guidelines) recommends all pts with AF should have rate control as first line unless what? (4)

A
  • There is a reversible cause for their AF (reverse cause and see if AF resolves)
  • The AF is of new onset (within last 48hrs. Can be heparinised and cardioverted using electrical or pharmacological cardioversion. Could be rate controlled instead though)
  • Heart failure thought to be primarily caused by AF/coexistent heart failure
  • They remain symptomatic despite being effectively rate controlled
  • Unstable/adverse features (as per ALS guidelines):
    • Shock
    • Syncope
    • Heart failure
    • Myocardial ischaemia
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17
Q

If a pt with atrial fibrillation has unstable/adverse features (shock, syncope, myocardial ischaemia or heart failure) what should you do?

A

Pt should be electrically cardioverted (as per the peri-arrest tachycardia guidelines)

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18
Q

State what drugs we can give to pts with AF for rate control

A
  • First line= beta blocker (e.g. atenolol 50-100mg once daily) or non-dihydropyridine CCB (e.g. diltiazem)
  • Digoxin (only in sedentary people/people who do little to no exercise- needs monitoring as risk of toxicity. May be beneficial if co-existent heart failure)

NICE state that if one drug doesn’t adequately control the rate than can use combination of 2 of the above.

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19
Q

Discuss the difference between immediate and delayed cardioversion including:

  • Who offered to
  • Any treatment required in mean time
A

Immediate Cardioversion

  • AF present for <48hr or pt severely haemodynamically unstable
  • Unlikley they have developed a blood clot in 48hr hence don’t need antiocoagulant prior to cardioversion

Delayed Cardioversion

  • AF present for >48hr and pt is stable
  • Pt needs to be anticoagulated for at least 3 weeks prior to cardioversion as they may have developed a clot in atria and reverting them back to sinus rhythm carries high risk of mobilising the clot causing a stroke. Pts should have rate control whilst waiting for cardioversion
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20
Q

What is an alternative strategy to anticoagulating patients with AF for >48hrs for 3 weeks prior to cardioversion?

A

Transoesophageal echo to exclude left atrial appendage

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21
Q

If there is a high risk of cardioversion failure, what is recommended?

A

Amiodarone or sotalol for at least 4 weeks prior to electrical cardioversion

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22
Q

State what two drugs can be used for pharmacological cardioversion

Describe what is involved in electrical cardioversion

A

Pharmacological Cardioversion

Agents with proven efficacy:

  • Flecainide (if no structural heart disease)
  • Amiodarone (drug of choice in pts with structural heart disease or co-existing heart failure)

Agents deemed less effective:

  • Beta blockers
  • CCBs
  • Digoxin
  • Procainamide

Electrical Cardioversion

  • Rapidly shock heart back into sinus rhythm (synchronised to R wave)
  • Give pt sedation or general anaesthetic and use cardiac defibrillator to deliver controlled shocks in attempt to restore sinus rhythm
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23
Q

Discuss whether anticoagulation is needed after electrical cardioversion of AF

A
  • If AF <48hrs and electrical cardioversion performed, anticoagulation is unnecessary
  • If AF >48hrs, anticoagulation for at least 4 weeks then reassess

*NOTE: NICE recommend electrical cardioversion if AF >48hrs

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24
Q

What drugs can be used for long term medical rhythm control if cardioversion is not an option

A
  • First line= beta blockers
  • Second line in patients following cardioversion= dronedarone
  • If pt have HF or LVD= amiodarone
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25
Q

What do NICE recommend considering if AF has not responded to or wish to avoid antiarrhythmic medications?

A
  • Percutaneous catheter ablation (can use radiofrequency or cryotherapy)
  • Anticoagulate for 4 weeks prior to procedure then after procedure for at least 2 months (duration depends on CHA2DVASC)
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26
Q

Discuss what treatment we can offer to pts with paroxysmal AF

A
  • Paroxysmal AF (arrhythmia self terminates within 7 days- but usually within 48hrs).
  • Offer pt “pill in pocket” approach; pt takes a pill to terminate AF when they feel the symptoms of AF starting
  • Flecanide is drug of choice
  • In order to be suited for pill in pocket approach pt needs to have:
    • Infrequent episodes
    • No underlying structural heart disease
    • Need to be able to identify when in AF
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27
Q

What score calculates stroke risk in patients with atrial fibrillation?

A
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28
Q

What do the following CHA2DVASC scores suggest regarding anticoagulation:

  • 0
  • 1
  • ≥ 2
A
  • 0 = no treatment
  • 1 = in MALES consider anticoagulation, in FEMALES no treatment
  • ≥2 = offer anticoagulation

**REMEMBER: if CHA2DVASC score suggests no need for anticoagulation must ensure transthoracic echo done to exclude valvular heart disease which in combination with AF is absolute indication for anticoagulation

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29
Q

What score do NICE recommend we use to calculate the risk of major bleed in patients on anticoagulation and is often used alongside CHA2DVASC score?

A

ORBIT SCORE (used to use hasbled)

30
Q

What medications are recommended for anticoagulation in AF?

A

DOACS are recommended first line e.g:

  • Apixaban
  • Rivaroxaban
  • Dabigatran
  • Edoxaban

(Warfarin is second line)

31
Q

What anticoagulation is recommended for patients with AF who have had a stroke?

A
  • Warfarin or direct factor Xa (e.g. rivaroxaban, apixaban) or direct thrombin inhibitor (e.g. dabigatran)
  • In absence of haemorrhage, start anticoagulation after 2 weeks
32
Q

State some potential complications of AF

A
  • Stroke
  • MI
  • Heart failure
33
Q

Explain how atrial fibrillation can lead to clot formation

A
  • Uncontrolled & disorgansied movement of atria leads to stagnation of lbood in left atrium- particularly in left atrial appendage
  • Stagnated blood leads to thrombus formation
  • Clot then mobilises (embolises)- atria to ventricle to aorta through carotids to brain where it can lodge in cerebral arteries & cause an ischaemic stroke
34
Q

Describe the pathophysiology of atrial flutter

A
  • Macro re-entrant loop in either atrium (usually in right atrium encircling the tricuspid annulus)
  • Electrical signal re-circulates in self-perpetuating loop (signal goes round and round atrium wihtout interuption)
  • Stimulates atria to contract at 300bpm
  • Due to refractory period of AV node, signal usually conducted to ventricles every second lap causing a ventricular rate of ~150bpm. This would give a 2:1 AV block however may aslo get 3:1 or 4:1 block. Very rarely in young beats every beat is conducted giving a 1:1 block (pt would be haemodynamiclaly compromised)
35
Q

State some risk factors/causes of atrial flutter

*Similar to atrial fibrillation

A
  • Pneumonia
  • Heart valve pathology
  • Ischaemic heart disease
  • Thyrotoxicosis
  • Heart failure
  • Hypertension
  • COPD
  • Asthma
36
Q

Why must you avoid flecainide in atrial flutter?

A

It can cause 1:1 AV conduction resulting in signigicatn tachycardia

37
Q

What investigations would you do if you suspect atrial flutter, include:

  • Bedside
  • Bloods
  • Imaging
A

Bedside

  • ECG: show atrial flutter

Bloods

  • FBC: raised WCC in infection
  • U&Es: assess electrolytes & can be helpful for choosing anti-arrhythmic
  • TFTs: thyrotoxicosis may present as atrial flutter
  • Cardiac enzymes: myocardial ischaemia may be cause of atrial flutter
  • NT-pro BNP: suspect heart failure as cause

Imaging

  • CXR: may show precipitating factor such as pneumonia, heart failure
  • ECHO: help identify cause e.g. valve pathology, heart failure
38
Q

Describe what you would see on the ECG of someone with atrial flutter

A
  • Rate: tachycardic (4:1, 3:1 or 2:1 block)
  • Rhythm: regularly irregular
  • P waves: sawtooth appearance on ECG
  • QRS: <120ms
39
Q

Discuss the treatment for atrial flutter

A

Treatment similar to AF

  • Haemodynamically unstable: electrical cardioversion
  • Haemodynamically stable:
    • Rate control e.g. beta blockers, CCBs, digoxin
    • Rhythm control (DC cardioversion preferred to pharmacological cardioversion)
    • Anticoagulation
  • If atrial flutter persists/failure of cardioversion:
    • Radiofrequency ablation of re-entrant rhythm (specifically radiofrequency ablation of tricuspid valve isthmus is curative for most pts)
40
Q

Describe what radiofrequency ablation of arrhythmias is

A
  • Give local or general anaesthetic
  • Pass catheter into femoral veins and pass through veins to heart under x-ray guidance
  • Once in heart, it is placed against different areas of heart to test electrical signals at at that point to try and find location of abnormal electrical pathways
  • Apply radiofrequency ablation (heat) to burn area
  • Leaves scar tissue that does not conduct electrical activity
41
Q

State some potential complications of atrial flutter

A
  • Stroke
  • Myocardial ischaemia
  • Heart failure
42
Q

What is meant by supraventricular tachycardias?

A
  • Supraventricular tachycardia means a tachycardia that is originating from above ventricles (this is the ‘technical defintion’). Hence this encompasses AF, atrial flutter, AVNRT, AVRT, atrial tachycardia..
  • In clinical practise, we refer to AF and atrial flutter by their names (AF and atrial flutter) and hence if an arrhythmia/ECG is referred to as SVT it means either AVNRT, AVRT or atrial tachycardia

“An arrhythmia consisting of rapid HR other than atrial fibrillation or flutter originating at or above the AV node”

43
Q

Discuss the pathophysiology of:

  • AVNRT
  • AVRT
  • Atrial tachycardia
A
  • AVNRT: electrical signal re-enters atria from ventricles via AV node. Once signal back in atria it travels back through AV node creating a self-perpetuating loop
  • AVRT: electrical signal re-enters atria from an accessory pathway that connects atria and ventricles. Once signal is back in atria it travels back to ventricles via AV nod creating self perpetuation loop (e.g. Wolff Parkinson White)
  • Atrial tachycardia: electrical signal originates in atria somewhere other than SA node; caused by abnormally generated activity in atria via atrial ectopics.
44
Q

State some symptoms of SVTs

A

Pt may be asymptomatic or may have:

  • Palpitations
  • Symptoms of heart failure e..g SOB, fatigue, orthopnonea
  • Symptoms of ischaemia e.g. chest pain, sweating, nausea
  • Symptoms of decreased cardiac output e.g. syncope
45
Q

Describe how SVT often appear on ECG

A
  • Rate= tachycardia
  • Rhythm= regular
  • Narrow QRS complex
  • Often can’t see p waves due to tachycardia. Looks like QRS, T wave, QRS, T wave etc… *NOTE: usually can’t see P waves but you might be able to

Mechanism for reading ECG:

  • Is it tachycardia?
  • Is QRS narrow?
  • Is it regular: if regular could be SVT or atriallfutter
  • Hard to distinguish between SVT or atrial flutter if HR fast
46
Q

Discuss the managemetn of SVTs in stable pts

A
  • First line= vagal manoeuvres (e.g. valsava manouevre & carotid sinus massage) to slow conduction at AV node; this can potentially interupt re-entrant circuit
  • If SVT not terminated by vagal manoeuvres give IV adenosine or verapamil
  • If the above fails, do direct current cardioversion
47
Q

Describe the following vagal manoeuvres:

  • Valsalva manoeuvre
  • Carotid sinus massage
A
  • Valsalva manoeuvre: get pt to take deep breath in, hold it, close mouth & pinch nostrils, bear down like going to toilet, blow out of nose (against pinched nose)
  • Carotid sinus massage: massage carotid sinus for few seconds on non-dominant cerebral hemisphere side. Wait at least 10 second before trying other side
48
Q

Who should you avoid doing a carotid sinus massage in and why?

A

Generally only do in young pts due to risk of stroke from emboli in elderly. Listen for carotid bruits before attempting this manoeuvre

49
Q

Describe how adenosine works in treatment of SVTs

A
  • Adenosine slows cardiac conduction primarily through AV node. It interrupts the AV node/accessory pathway during SVT and resets it back to sinus rhythm
  • Needs to be given as rapid bolus- followed by saline flush- as it has very short half life and need to ensure reaches heart ‘with enough impact to interrupt pathway’. Administered as a three way stopclock:
    • 6mg stat
    • If unsuccessful, further 12mg
    • If unsuccessful ,further 12mg
    • … follow this by long saline flush
50
Q

What must you warn a pt before you administer adenosine?

A
  • May produce chest discomfort
  • People describe it as it feels like you’re going to die
  • Reassure them that you have crash cart
51
Q

State some key points to remember when administering adenosine

A
  • Avoid in pts with asthma, COPD, heart failure, heart block, severe hypotension
  • Warn pt about feeling of dying/impeding doom
  • Give as fast IV bolus into large proximal cannula (grey cannula in antecubital fossa)
  • Have crash trolley next to pt
52
Q

What % of tachyarrhythmias due to AVNRT or AVRT does adenosine terminate?

If tachycardia continues despite some degree of AV blockade, what is the rhythm likely to be?

A
  • Adenosine terminates 90% of tachyarrhythmias due to AVNRT or AVRT
  • If tachycardia continues despite some degree of AV blockade rhythm is almost certainly atrial tachycardia or flutter; AVRT is excluded and AVNRT is very unlikely
53
Q

Verapamil IV can be given instead of rapid bolus of adenosine in attempt to treat SVT; state:

  • Dose of verapamil IV
  • Is it administered slow or fast
  • Who is must be avoided in
A
  • 5-10mg
  • Slowly
  • Avoid in pts already on beta blockers or in pts with known significatn LV dysfunction
54
Q

If vagal manoeuvres, adenosine and verapamil fail to terminate SVT what is the next option?

A

Synchronised electrical cardioversion under general anaesthetic or sedation

55
Q

Discuss the long term management of pts with paroxysmal SVT

A

Long term management of paroxysmal SVT is centred around preventing these episodes using:

  • Medication:
    • Beta blockers
    • CCBs (verapamil or diltiazem)
    • Flecanide
    • Amiodarone
  • Radiofrequency ablation
56
Q

Discuss the management of SVTs in unstable pts

A

Synchronised cardioversion following sedation starting at 150J

Unstable pts may have (as per ATLS peri-arrest guidelines):

  • Heart failure/pulmonary oedema
  • Shock (systolic <90mHg)
  • Chest pain with ischaemia
  • Syncope
57
Q

For Wolff-Parkinson White, describe:

  • What it is
  • ECG changes
  • Definitive treatment
A
  • Abnormal accessory pathway, Bundle of Kent, connecting atria & ventricles. In around half of cases, pathway only conducts retrograde (from ventricles to atria) and therefore doens’t alter appearnce of ECG in sinus rhythm- this is known as concealed acessory pathway. In other 50% of people with this pathway, pathway also conducts antegradely so impulse can travel from atria to ventricle via acessory pathway aswell as AV node- distorting QRS- this is known as a manifest pathway.
  • ECG:
    • Short PR interval
    • Wide QRS complex
    • Delta wave (slurred upstroke on QRS)
  • Definitive treatment= radiofrequency ablation
58
Q

Explain why most anti-arrhythmic are contraindicated in pts with WPW who also has AF or atrial flutter

A
  • If pt with WPW has atrial fibrillation or flutter there is a risk the chaotic electrical activity can pass through accessory pathway into ventricles causing polymorphic wide complex tachycardia
  • Most anti-arrhythmics increase risk of this by reducing condution through AV node and therefore promoting condution through acessory pathway hence they are contraindicated in WPW with atrial flutter or fibrillation
59
Q

Discuss the pathophysiology of ventricular tachycardia

State some risk factors for ventricular tachycardia

Describe the ECG changes

A
  • Due ventricular ectopics (usually due to activity in damaged tissue or re-entry in scarred ventricular tissue)
  • Two types:
    • Monomorphic
    • Polymorphic (torsades de pointes is a subtype of polymorphic VT)
  • RF: MI, coronary artery disease, cariomyopathy
  • Broad QRS complex tachycardia. May see capture beats (when p wave is conducted to ventricles producing normal sinus beat) or fusion beats (conducted impulse fuses with impulse from ventricles)

**AV dissociation is pathognomonic of ventricular tachycardia

60
Q

Why do we get concerned about ventricular tachycardia?

A

Potential to precipitate ventricular fibrillation

61
Q

Discuss the management of ventricular tachycardia in a:

  • Stable pt
  • Unstable pt
A

Stable

  1. Correct electrolyte problems
  2. Medical cardioversion e.g. with amiodarone. lidocaine, procainamide (DO NOT USE VERAPAMIL)
  3. Electrical cardioversion
  4. Implantable cardiac defibrillator

Unstable (shock, chest pain, heart failure)

  1. Immediate electrical cardioversion
62
Q

What medication MUST NOT be used for medical cardioversion of ventricular tachycardia?

A

Verapamil

63
Q

What is torsades de pointes, include:

  • What type of ventricular tachycardia it is
  • Pathophysiology
A
  • Polymorphic ventricular tachycardia
  • Occurs in pts with prolonged QT interval. Prolonged QT interval means there is prolonged repolarisation; prolonged repolarisation can result in random spontaneous depolarisations in some areas of heart myocytes. These abnormal depolarisations prior to repolarisation are called afterdepolarisations. Depolarisation spreads throughout ventricle causing contraction
64
Q

State some potential causes of prolonged QT

A
65
Q

Discuss the acute management of Torsades de Pointes

A
  • Correct underlying cause (electrolyte disturbances or remove medications)
  • IV magnesium sulphate (even if magnesium normal)
  • Defibrillation if VT occurs
66
Q

Discuss the long term management of torsades de pointes

A
  • Avoid medications that prolong QT
  • Correct electrolyte disturbances
  • Beta blockers (particularly sotalol)
  • Pacemaker or implantable defibrillator
67
Q

What are ventricular ectopic beats?

A

Premature ventricular beats caused by randome electrical discharges in ventricles

68
Q

What is bigeminy?

A

Ventricular ectopics are occuring so frequently that they happen after every sinus beat.

69
Q

Discuss the treatment of ventricular ectopics

A
  • Check bloods for anaemia, electrolyte disturbance, thyroid abnormalities
  • Reassurance & no treatment in otherwise healthy people
  • Seek advice in pts with background of heart conditions or other concerning features
70
Q

For Brugada syndrome, state:

  • Pathophysiology
  • ECG changes
  • Precipitants of ECG changes
A
  • Congenital condition in which there is a mutation in the Na+ channel gene- “sodium channelopathy”
  • ECG:
    • Coved ST segment elevation >2mm in >1 of V1-V3 and suggestive clinical history
  • Many people don’t have symptoms and don’t realise they have. Certain things can trigger symptoms such as fever, alcohol, medicaations, electrolyte imbalances. Symptoms can include: paplitations, SOB, dizziness, chest pains, blackouts, seizures. Suspect if someone in family suddenly died with no explanation

*NOTE: different types of brugada ECG pattern. This is type 1 pattern

71
Q

Discuss the management of bradycardia

A

Resus council say management depends on:

  1. ) Presence of adverse signs/haemodynamic compromise (heart failure, shock, chest pain/myocardial ischaemia, syncope)
  2. ) Risk of asystole

Management if adverse signs

  • First line= atropine 500mcg IV (can give up to maximum of 3mg)
  • Transcutaneous pacing
  • Adrenaline infusion titrated to response

Managing risk of asystole

Even if satisfactory response to atropine need specialist assessment to see if thre is need for transvenous pacing e.g. pt has complete heart block, Mobitz type II, recent asystole etc…

Yr3 Medicine- Cardiology (12 decks)

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